Component
Wernicke encephalopathy neurological symptoms
Clinical neurological manifestations assessed during treatment.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
In the 2016 case, neurological symptoms resolved after intravenous Mg was added to ongoing thiamine for documented hypomagnesemia.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Magnesium availability supports vitamin B1 activation or cofactor use in the specified preparation; this does not establish a dietary threshold or universal treatment failure.
- experimental_model
- Single 34-year-old man with alcohol withdrawal and Wernicke encephalopathy during intravenous thiamine treatment.
- limitations
- Single case during alcohol withdrawal; no controlled comparison or tissue-cofactor measurement.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- A patient improved with combined treatment after symptoms progressed during thiamine alone.
- primary_references
- [coughlan-2016-thiamine] Thiamine refractory Wernickes encephalopathy reversed with magnesium therapy (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5093844/ DOI: 10.1136/bcr-2016-218046
- tissue_or_cell_type
- Clinical neurological examination
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 759–769
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single 34-year-old man with alcohol withdrawal and Wernicke encephalopathy during intravenous thiamine treatment. · source_derived_draft · unverified_draft
### mg-thiamine-2016-neurologic-response In the 2016 case, neurological symptoms resolved after intravenous Mg was added to ongoing thiamine for documented hypomagnesemia. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A patient improved with combined treatment after symptoms progressed during thiamine alone. organism: Homo sapiens tissue_or_cell_type: Clinical neurological examination experimental_model: Single 34-year-old man with alcohol withdrawal and Wernicke encephalopathy during intravenous thiamine treatment. limitations: Single case during alcohol withdrawal; no controlled comparison or tissue-cofactor measurement. cross_nutrient: Magnesium availability supports vitamin B1 activation or cofactor use in the specified preparation; this does not establish a dietary threshold or universal treatment failure. [coughlan-2016-thiamine] Thiamine refractory Wernickes encephalopathy reversed with magnesium therapy (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5093844/ DOI: 10.1136/bcr-2016-218046
Complete structured claim and evidenceThe index infant had nystagmus, ophthalmoplegia, elevated lactate and abnormal transketolase activation despite normal brain MRI.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Results: Patient 1
- evidence_span
- Brain magnetic resonance imaging (MRI) revealed no abnormalities
- experimental_model
- Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging.
- exposure
- Consumption of a formula with thiamine below the assay detection limit
- limitations
- Single-patient diagnostic boundary; does not estimate MRI sensitivity or make every neurological symptom a thiamine-deficiency manifestation.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Homo sapiens
- plain_language
- Normal structural imaging did not exclude clinically important deficiency in this infant.
- primary_references
- [fattal-valevski-2005-formula-outbreak] Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. (2005). https://pubmed.ncbi.nlm.nih.gov/15687431/ DOI: 10.1542/peds.2004-1255
- tissue_or_cell_type
- Neurological examination and brain MRI
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1493–1505
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging. · source_derived_draft · unverified_draft
### thiamine-def-infant-normal-mri-boundary The index infant had nystagmus, ophthalmoplegia, elevated lactate and abnormal transketolase activation despite normal brain MRI. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal structural imaging did not exclude clinically important deficiency in this infant. organism: Homo sapiens tissue_or_cell_type: Neurological examination and brain MRI experimental_model: Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging. limitations: Single-patient diagnostic boundary; does not estimate MRI sensitivity or make every neurological symptom a thiamine-deficiency manifestation. evidence_location: Results: Patient 1 evidence_span: Brain magnetic resonance imaging (MRI) revealed no abnormalities exposure: Consumption of a formula with thiamine below the assay detection limit [fattal-valevski-2005-formula-outbreak] Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. (2005). https://pubmed.ncbi.nlm.nih.gov/15687431/ DOI: 10.1542/peds.2004-1255
Complete structured claim and evidence
Where it participates (unsigned role)
All three infants with ophthalmoplegia-related neurological manifestations had blood lactic acidosis; two also had high cerebrospinal-fluid lactate.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Results: three neurologically affected infants
- evidence_span
- All 3 had blood lactic acidosis
- experimental_model
- Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging.
- exposure
- Consumption of a formula with thiamine below the assay detection limit
- limitations
- The paper reports blood without specifying plasma in the accessible results. All nine infants had concurrent infections, so lactate is not a specific deficiency test.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Homo sapiens
- plain_language
- Severe infant deficiency could present with lactate accumulation alongside neurological signs.
- primary_references
- [fattal-valevski-2005-formula-outbreak] Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. (2005). https://pubmed.ncbi.nlm.nih.gov/15687431/ DOI: 10.1542/peds.2004-1255
- tissue_or_cell_type
- Blood and cerebrospinal fluid
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1479–1491
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging. · source_derived_draft · unverified_draft
### thiamine-def-infant-neurologic-lactate All three infants with ophthalmoplegia-related neurological manifestations had blood lactic acidosis; two also had high cerebrospinal-fluid lactate. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe infant deficiency could present with lactate accumulation alongside neurological signs. organism: Homo sapiens tissue_or_cell_type: Blood and cerebrospinal fluid experimental_model: Nine Israeli infants aged 2-12 months exposed to a defective soy-based formula in the 2003 outbreak; clinical examination, erythrocyte transketolase activation, lactate and selected neuroimaging. limitations: The paper reports blood without specifying plasma in the accessible results. All nine infants had concurrent infections, so lactate is not a specific deficiency test. evidence_location: Results: three neurologically affected infants evidence_span: All 3 had blood lactic acidosis exposure: Consumption of a formula with thiamine below the assay detection limit [fattal-valevski-2005-formula-outbreak] Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. (2005). https://pubmed.ncbi.nlm.nih.gov/15687431/ DOI: 10.1542/peds.2004-1255
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.